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Epigenetic Therapy in Breast Cancer

Yıl 2018, Cilt: 27 Sayı: 3, 346 - 362, 30.09.2018
https://doi.org/10.17827/aktd.365260

Öz

Cancer progression can be controlled by both genetic and epigenetic alterations. Only epigenetic alterations are reversible unlike the genetic alterations. This can be a important advantage to suggest that epigenetic modifications should be preferred in therapy applications. DNA methyltransferases and histone deacetylases have become the primary targets for studies in epigenetic therapy. The US Food and Drug Administration approved some DNA methylation inhibitors and histone deacetylation inhibitors as anti-cancer drugs. Therefore, the uses of epigenetic targets are believed to have great potential as a lasting favorable approach in treating breast cancer. 

Kaynakça

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  • 4. Alvarez RH. Present and future evolution of advanced breast cancer therapy. Breast Cancer Res.2010;12:S1.
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Meme Kanserinde Epigenetik Tedavi

Yıl 2018, Cilt: 27 Sayı: 3, 346 - 362, 30.09.2018
https://doi.org/10.17827/aktd.365260

Öz

Hem genetik hem de epigenetik değişikliklerle kanser ilerlemesi kontrol altına alınabilmektedir. Genetik değişimlerin geri dönüşümü imkansızken  epigenetik değişimler geri dönüştürülebilir. Bu avantaj, önerilen epigenetik modifikasyonların terapi uygulamalarında tercih edilmesi gerektiğini göstermektedir. DNA metiltransferaz ve histon deasetilaz epigenetik terapi çalışmalarının birinci hedefi haline gelmiştir. Bazı DNA metilasyon ve histon deasetilasyon inhibitörleri anti kanser ilaçları olarak Amerika’da Gıda ve İlaç İdaresi  tarafından onaylanmıştır. Bu nedenle, epigenetik hedeflerin kullanımları meme kanseri tedavisinde olumlu bir yaklaşım olarak büyük bir potansiyele sahip olduğuna inanılmaktadır.

Kaynakça

  • 1. Jemal A, Siegel R, Ward E, Hao Y, Xu J, Murray T, Thun MJ. Cancer statistics. Ca-Cancer J. Clin.2008;58:71–96.
  • 2. Kelly KM, Shah N, Shedlosky-Shoemaker R, Porter K, Agnese D. Living post treatment: Definitions of those with history and no history of cancer. J. Cancer Survivor. 2011;5:158–166.
  • 3. Taby R, Issa JP. Cancer epigenetics. Ca-Cancer J. Clin. 2010;60:376–392.
  • 4. Alvarez RH. Present and future evolution of advanced breast cancer therapy. Breast Cancer Res.2010;12:S1.
  • 5. Alvarez RH, Valero V, Hortobagyi GN. Emerging targeted therapies for breast cancer. J. Clin. Oncol.2010;28:3366–3379.
  • 6. Esteller M. Cancer epigenomics: DNA methylomes and histone-modification maps. Nat. Rev. Genet.2007;8:286–298.
  • 7. Handel AE, Ebers GC, Ramagopalan SV. Epigenetics: Molecular mechanisms and implications for disease. Trends Mol. Med. 2010;16:7–16.
  • 8. Egger G, Liang G, Aparicio A, Jones PA. Epigenetics in human disease and prospects for epigenetic therapy. Nature. 2004;429:457–463.
  • 9. Tahiliani M, Koh KP, Shen Y, Pastor WA, Bandukwala H, Brudno Y, Agarwal S, Iyer LM, Liu DR, Aravind L, et al. Conversion of 5-methylcytosine to 5-hydroxymethylcytosine in mammalian DNA by MLL partner TET1. Science. 2009;324:930–935.
  • 10. Robertson AB, Dahl JA, Vågbø CB, Tripathi P, Krokan HE, Klungland A. A novel method for the efficient and selective identification of 5-hydroxymethylcytosine in genomic DNA. Nucleic Acids Res.2011;39:e55.
  • 11. Voso MT, D’Alò F, Greco M, Fabiani E, Criscuolo M, Migliara G, Pagano L, Fianchi L, Guidi F, Hohaus S, et al. Epigenetic changes in therapy-related MDS/AML. Chem. Biol. Interact. 2010;184:46–49.
  • 12. Hatziapostolou M, Iliopoulos D. Epigenetic aberrations during oncogenesis. Cell. Mol. Life Sci.2011;68:1681–1702.
  • 13. Bestor TH. The DNA methyltransferases of mammals. Hum. Mol. Genet. 2000;9:2395–2402.
  • 14. Schaefer M, Hagemann S, Hanna K, Lyko F. Azacytidine inhibits RNA methylation at DNMT2 target sites in human cancer cell lines. Cancer Res. 2009;69:8127–8132.
  • 15. Chen ZX, Riggs AD. DNA methylation and demethylation in mammals. J. Biol. Chem.2011;286:18347–18353.
  • 16. Gehring M, Reik W, Henikoff S. DNA demethylation by DNA repair. Trends Genet. 2009;25:82–90.
  • 17. Cortez CC, Jones PA. Chromatin, cancer and drug therapies. Mutat. Res. 2008;647:44–51.
  • 18. Krawczyk B, Fabianowska-Majewska K. Alteration of DNA methylation status in K562 and MCF-7 cancer cell lines by nucleoside analogues. Nucleos. Nucleot. Nucleic Acids. 2006;25:1029–1032.
  • 19. Szyf M. Epigenetics, DNA methylation, and chromatin modifying drugs. Annu. Rev. Pharmacol. Toxicol. 2009;49:243–263.
  • 20. Chik F, Szyf M. Effects of specific DNMT gene depletion on cancer cell transformation and breast cancer cell invasion; toward selective DNMT inhibitors. Carcinogenesis. 2011;32:224–232.
  • 21. Mabaera R, Greene MR, Richardson CA, Conine SJ, Kozul CD, Lowrey CH. Neither DNA hypomethylation nor changes in the kinetics of erythroid differentiation explain 5-azacytidine’s ability to induce human fetal hemoglobin. Blood. 2008;111:411–420.
  • 22. Christman JK. 5-Azacytidine and 5-aza-2′-deoxycytidine as inhibitors of DNA methylation: Mechanistic studies and their implications for cancer therapy. Oncogene. 2002;21:5483–5495.
  • 23. Kuo HK, Griffith JD, Kreuzer KN. 5-Azacytidine induced methyltransferase-DNA adducts block DNA replication in vivo. Cancer Res. 2007;67:8248–8254.
  • 24. Li Q, Bartlett DL, Gorry MC, O’Malley ME, Guo ZS. Three epigenetic drugs up-regulate homeobox gene Rhox5 in cancer cells through overlapping and distinct molecular mechanisms. Mol. Pharmacol.2009;76:1072–1081.
  • 25. Qu Z, Fu J, Yan P, Hu J, Cheng SY, Xiao G. Epigenetic repression of PDZ-LIM domain-containing protein 2: Implications for the biology and treatment of breast cancer. J. Biol. Chem. 2010;285:11786–11792.
  • 26. Xu J, Zhou JY, Tainsky MA, Wu GS. Evidence that tumor necrosis factor-related apoptosis-inducing ligand induction by 5-Aza-2′-deoxycytidine sensitizes human breast cancer cells to adriamycin. Cancer Res.2007;67:1203–1211.
  • 27. Mirza S, Sharma G, Pandya P, Ralhan R. Demethylating agent 5-aza-2-deoxycytidine enhances susceptibility of breast cancer cells to anticancer agents. Mol. Cell Biochem. 2010;342:101–109.
  • 28. Beumer JH, Parise RA, Newman EM, Doroshow JH, Synold TW, Lenz HJ, Egorin MJ. Concentrations of the DNA methyltransferase inhibitor 5-fluoro-2′-deoxycytidine (FdCyd) and its cytotoxic metabolites in plasma of patients treated with FdCyd and tetrahydrouridine (THU) Cancer Chemother. Pharmacol.2008;62:363–368.
  • 29. Gowher H, Jeltsch A. Mechanism of inhibition of DNA methyltransferases by cytidine analogs in cancer therapy. Cancer Biol. Ther. 2004;3:1062–1068.
  • 30. Boothman DA, Briggle TV, Greer S. Exploitation of elevated pyrimidine deaminating enzymes for selective chemotherapy. Pharmacol. Ther. 1989;42:65–88.
  • 31. Yoo CB, Valente R, Congiatu C, Gavazza F, Angel A, Siddiqui MA, Jones PA, McGuigan C, Marquez VE. Activation of p16 gene silenced by DNA methylation in cancer cells by phosphoramidate derivatives of 2′-deoxyzebularine. J. Med. Chem. 2008;51:7593–7601.
  • 32. Billam M, Sobolewski MD, Davidson NE. Effects of a novel DNA methyltransferase inhibitor zebularine on human breast cancer cells. Breast Cancer Res. Treat. 2010;120:581–592.
  • 33. Balch C, Yan P, Craft T, Young S, Skalnik DG, Huang TH, Nephew KP. Antimitogenic and chemosensitizing effects of the methylation inhibitor zebularine in ovarian cancer. Mol. Cancer Ther.2005;4:1505–1514.
  • 34. Schuebel K, Baylin S. In living color: DNA methyltransferase caught in the act. Nat. Methods.2005;2:736–738.
  • 35. Brueckner B, Boy RG, Siedlecki P, Musch T, Kliem HC, Zielenkiewicz P, Suhai S, Wiessler M, Lyko F. Epigenetic reactivation of tumor suppressor genes by a novel small-molecule inhibitor of human DNA methyltransferases. Cancer Res. 2005;65:6305–6311.
  • 36. Fang MZ, Wang Y, Ai N, Hou Z, Sun Y, Lu H, Welsh W, Yang CS. Tea polyphenol (-)-epigallocatechin-3-gallate inhibits DNA methyltransferase and reactivates methylation-silenced genes in cancer cell lines. Cancer Res. 2003;63:7563–7570.
  • 37. Moyers SB, Kumar NB. Green tea polyphenols and cancer chemoprevention: Multiple mechanisms and endpoints for phase II trials. Nutr. Rev. 2004;62:204–211.
  • 38. Chen D, Milacic V, Chen MS, Wan SB, Lam WH, Huo C, Landis-Piwowar KR, Cui QC, Wali A, Chan TH, et al. Tea polyphenols, their biological effects and potential molecular targets. Histol. Histopathol.2008;23:487–496.
  • 39. Piña IC, Gautschi JT, Wang GY, Sanders ML, Schmitz FJ, France D, Cornell-Kennon S, Sambucetti LC, Remiszewski SW, Perez LB, et al. Psammaplins from the sponge Pseudoceratina purpurea: Inhibition of both histone deacetylase and DNA methyltransferase. J. Org. Chem. 2003;68:3866–3873.
  • 40. Atadja P, Gao L, Kwon P, Trogani N, Walker H, Hsu M, Yeleswarapu L, Chandramouli N, Perez L, Versace R, et al. Selective growth inhibition of tumor cells by a novel histone deacetylase inhibitor, NVP-LAQ824. Cancer Res. 2004;64:689–695.
  • 41. Davis AJ, Gelmon KA, Siu LL, Moore MJ, Britten CD, Mistry N, Klamut H, D’Aloisio S, MacLean M, Wainman N, et al. Phase I and pharmacologic study of the human DNA methyltransferase antisense oligodeoxynucleotide MG98 given as a 21-day continuous infusion every 4 weeks. Invest. New Drugs.2003;21:85–97.
  • 42. Stewart DJ, Donehower RC, Eisenhauer EA, Wainman N, Shah AK, Bonfils C, MacLeod AR, Besterman JM, Reid GK. A phase I pharmacokinetic and pharmacodynamic study of the DNA methyltransferase 1 inhibitor MG98 administered twice weekly. Annu. Oncol. 2003;14:766–774.
  • 43. Segura-Pacheco B, Trejo-Becerril C, Perez-Cardenas E, Taja-Chayeb L, Mariscal I, Chavez A, Acuña C, Salazar AM, Lizano M, Dueñas-Gonzalez A. Reactivation of tumor suppressor genes by the cardiovascular drugs hydralazine and procainamide and their potential use in cancer therapy. Clin. Cancer Res. 2003;9:1596–1603. 44. Zambrano P, Segura-Pacheco B, Perez-Cardenas E, Cetina L, Revilla-Vazquez A, Taja-Chayeb L, Chavez-Blanco A, Angeles E, Cabrera G, Sandoval K, et al. A phase I study of hydralazine to demethylate and reactivate the expression of tumor suppressor genes. BMC Cancer. 2005;5:44.
  • 45. Marsoni S, Damia G, Camboni G. A work in progress: The clinical development of histone deacetylase inhibitors. Epigenetics. 2008;3:164–171.
  • 46. Fang MH, Ji XM. Histone modification and its application in therapy for hematologic malignancies.Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2009;17:816–820.
  • 47. Namdar M, Perez G, Ngo L, Marks PA. Selective inhibition of histone deacetylase 6 (HDAC6) induces DNA damage and sensitizes transformed cells to anticancer agents. Proc. Natl. Acad. Sci. USA.2010;107:20003–20008.
  • 48. Candido EP, Reeves R, Davie JR. Sodium butyrate inhibits histone deacetylation in cultured cells. Cell.1978;14:105–113.
  • 49. Cho HJ, Kim SY, Kim KH, Kang WK, Kim JI, Oh ST, Kim JS, An CH. The combination effect of sodium butyrate and 5-Aza-2′-deoxycytidine on radiosensitivity in RKO colorectal cancer and MCF-7 breast cancer cell lines. World J Surg Oncol. 2009;7:49:1–49:7.
  • 50. Göttlicher M, Minucci S, Zhu P, Krämer OH, Schimpf A, Giavara S, Sleeman JP, Coco FL, Nervi C, Pelicci PG, et al. Valproic aciddefines a novel class of HDAC inhibitors inducing differentiation of transformed cells. EMBO J. 2001;20:6969–6978.
  • 51. Travaglini L, Vian L, Billi M, Grignani F, Nervi C. Epigenetic reprogramming of breast cancer cells by valproic acid occurs regardless of estrogen receptor status. Int. J. Biochem. Cell. Biol. 2009;41:225–234.
  • 52. Kim SH, Kang HJ, Na H, Lee MO. Trichostatin A enhances acetylation as well as protein stability of ERα through induction of p300 protein. Breast Cancer Res. 2010;12:R22.
  • 53. Li Y, Yuan YY, Meeran SM, Tollefsbol TO. Synergistic epigenetic reactivation of estrogen receptor-α (ERα) by combined green tea polyphenol and histone deacetylase inhibitor in ERα-negative breast cancer cells. Mol. Cancer. 2010;9:274.
  • 54. Stearns V, Zhou Q, Davidson NE. Epigenetic regulation as a new target for breast cancer therapy.Cancer Invest. 2007;25:659–665.
  • 55. Xu WS, Perez G, Ngo L, Gui CY, Marks PA. Induction of polyploidy by histone deacetylase inhibitor: A pathway for antitumor effects. Cancer Res. 2005;65:7832–7839.
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  • 62. Furumai R, Komatsu Y, Nishino N, Khochbin S, Yoshida M, Horinouchi S. Potent histone deacetylase inhibitors built from trichostatin A and cyclic tetrapeptide antibiotics including trapoxin. Proc. Natl. Acad. Sci. USA. 2001;98:87–92.
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  • 65. Keles E, Lianeri M, Jagodziński PP. Apicidin suppresses transcription of 17β-hydroxysteroid dehydrogenase type 1 in endometrial adenocarcinoma cells. Mol. Biol. Rep. 2011;38:3355–3360.
  • 66. Saito A, Yamashita T, Mariko Y, Nosaka Y, Tsuchiya K, Ando T, Suzuki T, Tsuruo T, Nakanishi O. A synthetic inhibitor of histone deacetylase, MS-27–275, with marked in vivo antitumor activity against human tumors. Proc. Natl. Acad. Sci. USA. 2009;96:4592–4597.
  • 67. Camphausen K, Burgan W, Cerra M, Oswald KA, Trepel JB, Lee MJ, Tofilon PJ. Enhanced radiation-induced cell killing and prolongation of gammaH2AX foci expression by the histone deacetylase inhibitor MS-275. Cancer Res. 2004;64:316–321.
  • 68. Srivastava RK, Kurzrock R, Shankar S. MS-275 sensitizes TRAIL-resistant breast cancer cells, inhibits angiogenesis and metastasis, and reverses epithelial-mesenchymal transition in vivo. Mol. Cancer Ther.2010;9:3254–3266.
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  • 72. Kelly TK, De Carvalho DD, Jones PA. Epigenetic modifications as therapeutic targets. Nat. Biotechnol.2010;28:1069–1078.
  • 73. Kristensen LS, Nielsen HM, Hansen LL. Epigenetics and cancer treatment. Eur. J. Pharmacol.2009;625:131–142.
Toplam 72 adet kaynakça vardır.

Ayrıntılar

Birincil Dil Türkçe
Konular Sağlık Kurumları Yönetimi
Bölüm Derleme
Yazarlar

Onur Eroğlu 0000-0002-3451-8540

Yayımlanma Tarihi 30 Eylül 2018
Kabul Tarihi 15 Şubat 2018
Yayımlandığı Sayı Yıl 2018 Cilt: 27 Sayı: 3

Kaynak Göster

AMA Eroğlu O. Meme Kanserinde Epigenetik Tedavi. aktd. Eylül 2018;27(3):346-362. doi:10.17827/aktd.365260